leprosy final.pptx

Topic for BAMS

1. LEPROSY (Hansen’s Disease)

2. INDEX Introduction History of leprosy Epidemiology Aetiology Classification Pathogenesis Transmission Incubation period Clinical features Treatment Reactions of leprosy MDT Management of leprosy

3. INTRODUCTION It is also known as Hansen’s disease . Leprosy is an chronic, granulomatous slowely progressive, distructive infection caused by Mycobacterium leprae. It mainly affects the peripheral nerves,skin and mucus membrane and resulting in deformities.

4. HISTORY Gerhard h enrik a rmauer hansen was a physician who idetified the Mycobacterium leprae as the cause of leprosy in 1873. India is considered the point of origin of leprosy with skeletal evidence of the disease dating to 2000 B.C. The disease is thought to have spread through trade and war to other parts of Asia, the Middle East, North Africa, and later Europe and the Americas. In ancient Indian society, individuals suffering from leprosy were alienated because the disease was chronic, contagious , resulted in disfigurement, had no cure at the time, and was associated with sin. Hansen (1841-1912)

5. EPIDEMIOLOGY According to the official reports recieved from 138 countries from all WHO regions,global registered prevelance of leprosy at the end of 2015,1,76, 176 cases (0.2 cases per 10,000 poeple). Leprosy currently affects approximately a quarter of a million people throughout the world, with majority of these cases being reported from India . Still, 1.2 to 1.3 hundred thousand new cases of leprosy reported every year, 58.8% of the total number of new cases reported every year.

6. ETIOLOGY It is caused by the Mycobacterium leprae . M.leprae is also known as the Hansen’s bacillus spirily . It is obligate intracellular paracite. Gram +ve bacteria. Shape – slender ,lightly curved Size – 1-8 micro(long) 0.3-1 micro(wide) Weakly acid fast bacteria Can not be cultured

7. Ridley and Jopling’s classification : Depends on clinico pathological spectrum of disease , determined by the immune resistance of the host. a. Tuberculoid leprosy (TT) – Show maximum immune response. b. Borderline tuberculoid (BT) – Immune response falls between the BB and BT. c. Borderline leprosy (BB) – Immune response falls between BT and BL. d. Borderline lapromatous (BL) – Immune response falls between BB and LL. e. Lapromatous leprosy (LL) – Least immune response. WHO Classification : 1.Paucibacillary leprosy : All cases of tuberculoid and some cases of borderline type. 2.Multibacillary leprosy : All cases of lepromatous leprosy and some cases of borderline type.

8. PATHOGENESIS OF LEPROSY

9. CLINICAL FEATURES TUBERCULOID LEPROSY Skin lesions : Number : single or few Site : usually face,trunk and extremities Types : localised,hypopigmented,red or pale in colour Numbness and loss of temperature in skin Amputation of fingers or toes Paralysis of eyelids,keratinitis and corneal ulcerations

10. LEPROMATOUS LEPROSY Lesions of skin : Number : multiple site : common at cooler areas of skin ( ear lobes,wrist, elbows , knees ,feet ) than warmer areas ( e.g. groin ,axilla). Type : macular, papular, or nodular, symmetric,hypoaesthetic LEONINE FACIES - When the nodular lesions of face and earlobes get coalesce to produce a lion like face. Loss of eye brows Pendulous ear lobes Claw hand Saddle nose Particularly the ulnar and paroneal nearves are invaded by the mycobacterium. Blindness : Anterior chamber of the eye is damaged Chronic nasal discharge

11. MODE OF TRANSMISSION Transmission by inhalation Droplet infecton (most common) Transmission by contact Skin to skin contact with infectious person Contact with soil or fomites Other routes Insects vectors e.g. Mosquito, Bed bugs Tatting needles Breast feeding and transplacental infection do not occure. INCUBATION PERIOD : Tuberculoid Leprosy : 2-5 yr Lepromatous Leprosy : 8-12 yr

12. INVESTIGATION Sensory testing Peripheral nerve examination Demonstration of acid fast bacilli Skin smears - slit / scrape method Nasal swab - Ziehl-Neelsen stain method Molecular method : Polymerase chain reaction (PCR). LEPROMIN TEST : It is not a diagnostic test . Method : Lepromin ( the antigen extract of M. Leprae) is injected intradermally Reaction : Fernandez reaction : Early 9 24-48 hr ) and positive reaction Mistuda reaction : Delayed granulomatous reaction ( 3-5 weeks) Uses : 1. Classification of leprosy 2. Evaluation of cellmediated immunity status in patient 3. Know the prognosis

13. Reactions in leprosy The immunity in leprosy may change spontaneously or following treatment. • Type I reaction : – Borderline leprosy is the most unstable form of leprosy where immune status may shift up or down. These are called as type I reaction, which may be of two types : Upgrading reactions : If immunity improves , the disease may shift towards tuberculoid leprosy. Downgrading reaction : If the immunity decreases , the disease moves towards lepromatous leprosy. • Type II reaction ( erythema nodosum leprosum ) – It occurs in mostly in lepromatous leprosy, particularly when on treatment. – Clinical features : 1) Tender red plaque or nodules and 2) fever, malaise and arthralgia(joint pain)

14. Treatment of leprosy Dapsone (DDS) : Diamino diphenyl sulfone Clofazimine Rifampicin Ofloxacin Minocycline

15. Treatment of immunologic reactions Type I reactions Clofazimine 200mg daily Corticosteroids (Prednisolone) Rest Type II reactions Corticosteroids Prednisolone Thalidomide – 100 -300 mg/day ** avoided during pregnancy and lactation Rest

16. MDT MDT(Multi Drug Therapy) is a key element for cure. MDT is free of charge from WHO (From 1981). Drug used in WHO-MDT are : Rifampicine,clofazimine and Dapsone –MB Rifampicine and Dapsone – PB Treatment of leprosy with only single drug will always result in development of drug resistance

17. Management of leprosy In 2016 WHO has launched a new global leprosy strategy – The Global Leprosy Strategy 2016-2020 accelerating towards a leprosy free world. India is currently running a leprosy eradication National Leprosy Eradication Programme(NLEP) since 1983. c cf

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